miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.

Oxidative stress has been shown to contribute to the development of age-related macular degeneration (AMD). MicroRNAs (miRNA) are small non-coding RNA molecules that function in RNA silencing and post-transcriptional regulation of gene expression. We showed miR-17-3p to be elevated in macular RPE ce...

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Main Authors: Bo Tian, Daniel E Maidana, Bernard Dib, John B Miller, Peggy Bouzika, Joan W Miller, Demetrios G Vavvas, Haijiang Lin
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2016-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4978424?pdf=render
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spelling doaj-21db63b9db254049b45e382e8b0cba042020-11-25T00:08:36ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-01118e016088710.1371/journal.pone.0160887miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.Bo TianDaniel E MaidanaBernard DibJohn B MillerPeggy BouzikaJoan W MillerDemetrios G VavvasHaijiang LinOxidative stress has been shown to contribute to the development of age-related macular degeneration (AMD). MicroRNAs (miRNA) are small non-coding RNA molecules that function in RNA silencing and post-transcriptional regulation of gene expression. We showed miR-17-3p to be elevated in macular RPE cells from AMD patients and in ARPE-19 cells under oxidative stress. Transfection of miR-17-3p mimic in ARPE-19 induced cell death and exacerbated oxidative lethality that was alleviated by miR-17-3p inhibitor. The expression of antioxidant enzymes manganese superoxide dismutase (MnSOD) and thioredoxin reductase-2 (TrxR2) were suppressed by miR-17-3p mimic and reversed by miR-17-3p inhibitor. These results suggest miR-17-3p aggravates oxidative damage-induced cell death in human RPE cells, while miR-17-3p inhibitor acts as a potential protector against oxidative stress by regulating the expression of antioxidant enzymes.http://europepmc.org/articles/PMC4978424?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Bo Tian
Daniel E Maidana
Bernard Dib
John B Miller
Peggy Bouzika
Joan W Miller
Demetrios G Vavvas
Haijiang Lin
spellingShingle Bo Tian
Daniel E Maidana
Bernard Dib
John B Miller
Peggy Bouzika
Joan W Miller
Demetrios G Vavvas
Haijiang Lin
miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.
PLoS ONE
author_facet Bo Tian
Daniel E Maidana
Bernard Dib
John B Miller
Peggy Bouzika
Joan W Miller
Demetrios G Vavvas
Haijiang Lin
author_sort Bo Tian
title miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.
title_short miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.
title_full miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.
title_fullStr miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.
title_full_unstemmed miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.
title_sort mir-17-3p exacerbates oxidative damage in human retinal pigment epithelial cells.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2016-01-01
description Oxidative stress has been shown to contribute to the development of age-related macular degeneration (AMD). MicroRNAs (miRNA) are small non-coding RNA molecules that function in RNA silencing and post-transcriptional regulation of gene expression. We showed miR-17-3p to be elevated in macular RPE cells from AMD patients and in ARPE-19 cells under oxidative stress. Transfection of miR-17-3p mimic in ARPE-19 induced cell death and exacerbated oxidative lethality that was alleviated by miR-17-3p inhibitor. The expression of antioxidant enzymes manganese superoxide dismutase (MnSOD) and thioredoxin reductase-2 (TrxR2) were suppressed by miR-17-3p mimic and reversed by miR-17-3p inhibitor. These results suggest miR-17-3p aggravates oxidative damage-induced cell death in human RPE cells, while miR-17-3p inhibitor acts as a potential protector against oxidative stress by regulating the expression of antioxidant enzymes.
url http://europepmc.org/articles/PMC4978424?pdf=render
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